To overcome Iraqi forces, coalition troops fired thousands
of shells tipped with DU. But we still don'tfully understand its
long-term health effects

DUNCAN GRAHAM-ROWE

WRECKED tanks and vehicles litter the Iraqi countryside. Ruined
buildings dominate towns and cities. Many were blown to pieces
by shells tipped with depleted uranium, a material that the US
and Britain say poses no long-term health or environmental risks.
But many Iraqis, and a growing band of scientists, are not so
sure. Last week, the UN Environment Programme (UNEP) announced
it wanted to send a scientific team into Iraq as soon as possible
to examine the effects of depleted uranium (DU). People's fears
that DU leaves a deadly legacy must be addressed, says UNEP. Some
scientists go further. Evidence is emerging that DU affects our
bodies in ways we do not fully understand, they say, and the legacy
could be real. DU is both radioactive and toxic. Past studies
of DU in the environment have concluded that neither of these
effects poses a significant risk. But some researchers are beginning
to suspect that in combination, the two effects could do significant
harm. Nobody has taken a hard look at the combined effect of both,
says Alexandra Miller, a radiobiologist with the Armed Forces
Radiobiology Research Institute in Bethesda, Maryland. "The
bottom line is it might contribute to the risk." She is not
alone. The idea that chemical and radiological damage are reinforcing
each other is very plausibleandgainingmomentum, says Carmel Mothersill,
head of the Radiation and Environmental Science Centre at the
Dublin Institute of Technology in Ireland. "The regulators
don't know how to handle it. So they sweep it under the carpet."
A by-product of the uranium enrichment process, DU is chemically
identical to natural uranium. But most of the 235 isotope has
been extracted leaving mainly the non-fissionable 238 isotope.
It is used to make the tips of armour-piercing shells because
it is extremely dense: 1.7 times as dense as lead.

"In 1991, an estimated 350 tonnes of DU was fired at Iraqi
tanks. That figure is likely to be matched in the current conflict"

Also, unlike other heavy metals that tend to flatten, or mushroom,
upon impact, DU has the ability to "self-sharpen" as
material spread out by the impact ignites and bums off as the
munition pierces its target. During the Gulf war in 1991, the
US and Britain fired an estimated 350 tonnes of DU at Iraqi tanks,
a figure likely to be matched in the course of the current conflict.
In the years since then, doctors in southern Iraq have reported
a marked increase in cancers and birth defects, and suspicion
has grown that they were caused by DU contamination from tank
battles on farmland west of Basra. As the Pentagon and the Ministry
of Defence point out, this claim has not been substantiated. Iraq
did not allow the World Health Organization to carry out an independent
assessment. Given its low radioactivity and our current understanding
of radiobiology, DU cannot trigger such health effects, the British
and American governments maintain. But what if they are wrong?
Though DU is 40 per cent less radioactive than natural uranium,
Miller believes that its radiological and toxic effects might
combine in subtle, unforeseen ways, making it more carcinogenic
than thought. it's a controversial theory, but one for which Miller
has increasing evidence. Uranium is "genotoxic" ' It
chemically alters DNA, switching on genes that would otherwise
not be expressed. The fear is that the resulting abnormally high
activity in cells could be a precursor to tumour growth. But while
the chemical toxicity of DU is reasonably well established, Mothersill
points out that the radiological effects of DU are less clear.
To gauge the risk from low-dose radiation, researchers extrapolate
from tests using higher doses. But the relationship between dose
and effect is not linear: at low doses radiation kills relatively
fewer cells. And though that sounds like good news, it could mean
that low radiation is having subtle effects that go unnoticed
because cells are not dying, says Mothersill. Miller has found
one way this may happen. She has discovered the first direct evidence
that radiation from DU damages chromosomes within cultured cells.
The chromosomes break, and the fragments reform in a way that
results in abnormal joins (Milita?y Medicine, vol 167, p 120).
Both the breaks and the joins are commonly found in tumour cells.
More crucially, she has recently found that DU radiation increases
gene activity in cultured cells at doses of DU not known to cause
chemical toxicity (Molecular and CellularBiochemistry, in press).
The possible consequences are made all the more uncertain because
no one knows if genes switched on by DU radiation enhance the
damage caused by genes switched on by DU's toxic effects, or vice
versa. "I think that we assumed that we knew everything that
we needed to know about uranium," says Miller. "This
is something we have to consider now when we think about risk
estimates." Britain's Royal Society briefly referred to these
synergistic effects in its report last year on the health effects
of DU munitions. "There is a possibility of damage to DNA
due to the chemical effects being enhanced by the effects of the
alpha-particle irradiation." But it makes no recommendations
for future research to evaluate the risks.

"There is a danger that laboratory experiments not specifically
looking for this erred could miss animportant source of damage"

The bystander effect

Miller points to another reason to be concerned about DU: the
so-called "bystander effect". There is a growing consensus
among scientists that radiation damages more than just the cells
it directly hits. In tests using equipment that allows single
cells to be irradiated by individual alpha particles, gene expression
increases both in irradiated cells, and in neighbouring cells
that have not been exposed. "At high doses, 'bystander'is
not an issue because you are killing so many cells. But at low
doses that's not really true," says Miller. There is a danger
that experiments not specifically looking for this effect could
miss an important source of damage. A body of research has also
emerged over the past decade showing that the effects of radiation
may not appear immediately. Damage to genes may be amplified as
cells divide, so the full consequences may only appear many generations
after the event that caused it. And while the chemical toxicity
of DU itself is more clear-cut, the possibility remains

that there may still be some unforeseen synergistic effects
at a genetic level. Other heavy metals, such as tungsten, nickel
and cobalt are similarly genotoxic. When Miller and her team exposed
human cells to a mixture of these metals, significantly more genes
became activated than when the cells were exposed to the equivalent
amount of each metal separately (Molecular and CellularBiochemistry,
in press). Miller and Mothersill say that recommended safe radiation
limits are often based on the idea that only irradiated cells
will be affected, and ignore both the bystander effect and the
possible amplification over the generations. "Nothing should
be written in stone when it comes to risk assessment," agrees
Michael Clark at Britain's National Radiological Protection Board.
But even if there were a case for re-evaluating the dosimetry
for low-dose radiation, he says we should be cautious of the significance
of Miller's lab-based research. "An in vitro effect is not
a health effect." Also, says Clark, everyone has traces of
natural uranium in their bodies. "If there was some sort
of subtle low-dose effect I think we would have seen it,"
he says. Because none has shown up in epidemiological studies,
it seems unlikely there are any health effects associated with
DU, which is less radioactive. But Miller is not convinced. While
most people have small amounts of uranium in their bodies, she
says no studies have been done to see whether this contributes
to cases of cancer in society at large. The military tends to
dismiss such hazards as being of only theoretical significance,
at least when it comes to civilians. According to the Pentagon,
the only risk of exposure is during combat, when DU shells hit
hard targets and the metal ignites. This creates clouds of uranium
oxide dust that can be breathed in. But heavy oxide particles
quickly settle, it says, limiting the risk of exposure. "A
small dust particle is still very heavy," says Michael Kilpatrick
of the US Deployment Health Support Directorate. "It stays
on the ground." That sounds reassuring until you read UNEP's
latest report on DU left over from conflicts in former Yugoslavia
in the mid-iggos. Last month, a team of experts collaborating
with the International Atomic Energy Agency, WHO and NATO concluded
that DU poses little risk in Bosnia although it can still be detected
at many sites. just 11 tonnes was fired in that conflict. But
evidence that DU may be moving through the ground and could contaminate
local water supplies should be investigated further, UNEP says.
And on rare occasions, wind or human activity may raise DU-laden
dust that local people could inhale. The Royal Society admits
that localised areas of DU contamination pose a risk, particularly
to young children, and should be cleared up as a priority. They
also recommend the environmental sampling of affected areas (see
"Royal Society Reports on DU, 2002", below). Such evidence
is partly why UNEP is keen to study DU flred during the present
conflict in Iraq. Assessments in former Yugoslavia were made up
to seven years after DU weapons were used, UNEP admits, and a
more immediate study in Iraq would give us a much better understanding
of how DU behaves in the environment. Any hazards such a study
identifies could be dealt with immediately, says UNEP. And even
now, an investigation in Iraq could reveal risks remaining from
DU fired during the Gulf war in 1991.

Veterans show ill effects

Cracks are also appearing in the argument that DU munitions
have not proven harmful even to troops. In the 1991 war, more
than 100 coalition troops were exposed to DU after being accidentally
fired on by their own forces. The majority inhaled uranium oxide,
while the rest suffered shrapnel injuries. Some still have DU
in their bodies. Britain and America point out that none has developed
cancers or kidney problems, as might have been expected if DU
posed a long-term danger. But researchers at the Bremen Institute
for Prevention Research, Social Medicine and Epidemiology in Germany
have found that all is not well with the veterans. Last month
they published results from tests in which they took blood samples
from 16 of the soldiers, and counted the number of chromosomes
in which broken strands of DNA had been incorrectly repaired.
In veterans, these abnormalities occurred at five times the rate
as in a control group Of 4o healthy volunteers (Radiation Protection
Dosimetry, vol 103, p 211). "Increased chromosomal aberrations
are associated with an increased incidence of cancers," says
team member Heike Schr6der. The damage occurred, they say, because
the soldiers inhaled DU particles in battle. The NRPB is unconvinced.
"It is possible that exposure to significant amounts of DU
could cause excess chromosome aberrations, but this study has
technical flaws," says Clark. "There are no proper controls
to compare results with soldiers who were not exposed to DU. And
some of the reported excess aberrations are well known to be linked
to chemicals rather than radiation."

"An immediate study in Iraq would give us a much better
understanding of how DU behaves in the environment"

Tough decision to make Deciding whether DU is to blame will
be tough. Independent research may confirm that rates of cancer
have increased in the Iraqi population. But the Iraqi government
has used chemical weapons on its own people that can produce the
same outcome, and it is impossible to know for sure who may have
been exposed. Soldiers may similarly have been exposed to chemicals
in iggi. The only way to resolve the issue is more research, says
Dudley Goodhead, director of Britain's Medical Research Council's
Radiation and Genome Stability Unit at Harwell, near Oxford."Ijtls
something important that needs to be explained." Miller admits
it is entirely possible that DU contamination is safe. But many
of the scientific investigations into DU have only just begun,
and their results will be long coming."None of this has been
looked at or even thought about it until the last few years,"
she says. As the dust begins to settle in Iraq, it remains to
be seen when the ravages of war will end. Additional reporting
by Rob Edwards 0

Slow farewell twixt man and ape

HUMANS and chimpanzees did not gradually evolve into different
species by living geographically apart, as textbooks suggest.
Our isolation from chimps occurred within our own chromosomes,
not across the plains of Africa, says a team who compared human
and chimp DNA. The study gives rise to the theory that the chromosomes
of our common ancestors became accidentally rearranged during
reproduction, and this gradually led to genetic "no-go"
zones between protohumans and proto-chimps. The two could still
mate, and swap genes between compatible parts of their chromosomes,
but any mutations within non-compatible regions that conferred
an evolutionary advantage would have been retained for good by
each lineage. "It became utterly impossible to swap genes
between those zones, so they became areas where you had increasingly
separated gene pools," says Arcadi Navarro of the Pompeu
Fabra University in Barcelona, who co-analysed the DNA with Nick
Barton of the University of Edinburgh. The implications are huge.
First, it means the parting of the ways between human and chimp
was much more gradual than previously believed. Instead of the
sharp division brought about by geographic separation, common
ancestors destined to become either chimps or humans were able
to interbreed with each other until their chromosomes were no
longer compatible. Secondly, and more controversially, it means
that the common ancestors of both species gradually diverged from
one another despite sharing the same habitat and territory. "It
might explain discrepancies in anthropological data about the
time and location of divergence," says Christophe Soligo
of the human origins research group at the Natural History Museum
in London. "It implies there was a longer period of hybridisation
than thought."

Humans have lo chromosomes that have undergone different rearrangements
to those of chimps In 9 of these there are pericentric inversions
- essentially a swapping of two large pieces of the chromosome
around the centromere. The loth was created by the fusion of two
smaller chromosomes, which remain separate in chimps (see Graphic).
Navarro and Barton compared DNA from 115 genes, half of which
sit on regions of the chromosomes useful mutations can be retained
and evolve, backing the hunch that this is the genetic engine
driving development of separate species (Science, VOI 300, P 321).
"They are probably the genes that made the two species incompatible,
producing traits that eventually stopped them choosing each other
as mates," says Navarro. Other researchers have tried unsuccessfully
to implicate chromosomal isolation as the driving force for the
development of different species. Their ideas foundered, says
Navarro, because chromosomal rearrangements were thought to either
be lethal to the recipient, or to render them infertile. However,
experiments in fruit flies and sunflowers over the past decade
have shown organisms can survive with rearranged chromosomes,
which are then passed down the generations. The divergence eventually
prevents the exchange of genes and they become separate species.
"For the first time it provides a plausible explanation for
how speciation might have taken place without geographical or
ecological separation," says Soligo.

that are rearranged differently in humans and chimps, and half
on "colinear" chromosomal regions common to the two
species. Although gene mutations occur at the same rate in both
ordinary and rearranged chromosomes, the researchers found that
mutations accumulated twice as often in the rearranged segments.
In essence, they are a refuge within which

Worms and Ageing

"AT ITS most extreme, we were accused of fraud,"
recalls biologist Tom Johnson. Fifteen years ago, he and colleague
David Friedman, both then at the University of California, Irvine,
announced a result that contradicted everything biologists thought
they knew about ageing and lifespan. They showed that a change
in a single gene was responsible for making nematode worms live
up to 65 per cent longer than normal. The finding was greeted
with intense scepticism. Critics were vehement: a creature's lifespan
couldn't possibly be manipulated so easily because ageing was
not controlled by genes. Rather, it was simply a product of random,
uncontrolled degeneration. To suggest otherwise was to imply that
evolutionary theorists were completely wrong in what they believed
about ageing. But since then, critics have had to eat their words
as a growing body of results threatens to demolish long-standing
theories of how and why we age. Scientists have come to accept
that simple organisms such as flies and worms possess a simple
switch that dictates lifespan. Some are even convinced that this
switch works through a handful of molecular signals that affect
the rate of ageing. In January this year came an even more surprising
result. French researchers revealed that mammals possess a similar
switch. They unveiled a single-gene mutation that extends longevity
in mice via a molecular pathway similar to the one in the worm.
This surprise finding is being hailed as powerful evidence that
all animals have a genetic switch that can alter normal lifespan.
The idea that lifespan has an inbuilt, genetically controlled
flexibility has sparked a spirited debate. Some researchers believe
such results fit nicely with existing theories of how and why
we age but others argue it will force a major rethink. "It's
quite clear that this pathway is regulating the rate of ageing,"
says Cynthia Kenyon, a geneticist at the University of California,
San Francisco, and one of the leaders in the study of the genetics
of ageing. What's more, she adds, human intervention could alter
this pathway.

The main bone of contention is that if genes do control the
rate of ageing, they must have somehow evolved for this purpose
by natural selection. And for decades, evolutionary biologists
were convinced that genes specifically for ageing couldn't have
evolved, because the process starts after an organism has successfully
reproduced and should therefore lie beyond the reach of natural
selection. Leonard Hayflick, a gerontologist at the University
of California, San Francisco - famous for his discovery that human
cells cannot divide indefinitely - is firmly in this camp. Last
year, he released a letter signed by 51 scientists warning the
public against the notion of an ageing program that could be manipulated.
"Ageing is not, as some might think, a genetically programmed
process, playing itself out on a rigidly predetermined schedule,"
wrote Hayflick and his co-authors. "The way evolution works
makes it impossible for us to possess genes that are speciflcauy
designed to cause physiological decline with age, or to control
how long we live.' The idea that ageing and death are evolved
traits was first mooted after Darwin outlined his theory of evolution
in 1859. Alfred Russel Wallace, who came up with the idea of natural
selection at around the same time, suggested that individuals
are programmed to die so as not to compete with their offspring,
an argument expanded by influential German biologist August Weismann.
But students of evolution later concluded this made little sense.
For one thing, animals consistently live much longer in captivity.
How could they have evolved a genetic program that never gets
used in the wild? Secondly, if a death program did exist, selection
would likely favour individuals who acquired genetic mutations
that allowed them to escape that program, live longer and so have
the chance of producing more offspring. By the time of his death
in 1914, Weismann had largely changed his mind. In the 1920S,
programmed ageing was dismissed as a "perverse extension
of the theory of natural selection". Current explanations
for why ageing occurs first emerged in the late 1940s when Peter
Medawar began formulating his "mutation accumulation"
theory. According to Medawar, genes that have a negative impact
on health only late in life will tend to accumulate in the genome
due to the absence of selective pressure to remove them. Take
Huntington's disease, for example. This genetic disorder is deadly,
but since its effects usually only begin to occur when carriers
are in their 30s or 40s, the gene has already been passed on to
the next generation. In 1957 noted American evolutionary biologist
George Williams added a twist to this theory. According to Williams,
ageing results from natural selection favouring mutations that
bestow advantage to an individual early in life - regardless of
the negative effects these same genes may have after reproduction
is over. For example, Williams suggested that selection would
favour a gene that helped calcify bones to make them stronger
early in life, even if it meant calcification in arteries later
on in life.

Balancing act In the late 1970s, gerontologist Tom Kirkwood,
now at the University of Newcastle upon Tyne, built on Williams's
notion that ageing is the result of a trade-off. According to
Kirkwood, an organism has only a limited budget of energy to divide
between reproduction and maintaining its own tissues. The result
is a trade-off, with the organism diverting energy to reproduction
and neglecting maintenance, resulting in ageing. The extent and
pattem of this energy diversion will be dictated by a species'ecological
circumstances. Mice, for example, live in harsh conditions and
are the favourite meal of many a predator. Their need to invest
in early and frequent reproduction helps explain their short lifespan.
By the ig8os, as the revolution in molecular biology was helping
researchers unravel the genetic pathways underlying complex processes
such as embryonic development and growth, gerontologists were
being told not to bother. Johnson's discovery that a single gene
named age-1 altered the longevity of worms was not only doubted,
it was downright ignored. But then, in 1993, Kenyon described
a second longevity gene in worms, daf-2. This finding turned heads,
partly because daf-2 had an even more dramatic impact on lifespan
than age-1 - mutant worms lived on average twice as long as normal
- and partly because the gene was known to be involved in sending
worms into a weird physiological state called a dauer larva. Prior
to adulthood, juvenile worms can enter this state in response
to starvation. They stop growing and developing, and store extra
fat and seal themselves up at both ends. This delay in their development
can extend their normal two-week lifespan by months. Kenyon found
that by altering the expression of daf-2 just a little, worms
lived longer without becoming dauers. This raised the possibility
that the extended lifespan was independent of the other changes
associated with the dauer state. This finding took on greater
significance in 1997 when scientists at Harvard Medical School
in Boston cloned daf-2 and discovered that it codes for a worm
version of the human insulin receptor, a molecule used for transporting
insulin into cells that is key to regulating energy metabolism.
For longevity researchers, this was an intriguing development.
Since the 193os researchers have known that lab animals will live
much longer when their calorie intake is restricted - 50 per cent
longer in the case of rats. The same has been seen in species
ranging from yeast to dogs. The parallels between long-lived daf-2
worm mutants and calorie- restricted animals suggested that Kenyon
had found part of a molecular pathway that affects lifespan in
most, if not all, animals. These discoveries in worms were followed
by others showing that alterations to genes with similar functions
in yeast and fruit flies also extended lifespan. January's big
news, from a research team led by Yves Le Bouc at the Institute
of Health and Medical Research in Paris, came from experiments
on mice in which another insulin-related signalling pathway had
been disabled. In this instance it was the insulin-like growth
factor-1 (IGF-1) pathway, which regulates many functions including
energy metabolism. In the mouse experiments, knocking out the
pathwayextended average longevity bY 33 per cent in females and
16 per cent in males. It looked as though insulin-related pathways
were involved in ageing in a mammals, too. "This finding
is the most definitive evidence yet that this really is an evolutionarily
conserved pathway," says Johnson.

"The long-lived mice provide the most definitive evidence
yet thatthesegenes have been conserved throughout evolution"

Assuming that this system exists in most animals, how might
it work? How could just a few genes affect the duration of life?
The mutant animals created by researchers such as Kenyon seem
to be more resistant to cellular damage, and accumulated damage
is believed to be the main cause of ageing. Numerous studies show
that virtually every one of these long-lived animals is better
at avoiding the kind of cellular damage normally caused by exposure
to chemicals, extreme temperature and UV radiation. Could these
signalling pathways damp down the activity of cellular repair
machinery, and so promote ageing? Evidence to support this idea
comes from the finding that worms with a mutant daf-2 gene lose
their life-extension if they also lack parts of their damage repair
machinery. Cells have a range of proteins and molecules that protect
them from damage - such as the antioxidant enzyme superoxide dismutase
They also come equipped with repair mechanisms to undo damage
after the fact (New Scientist, 15 March, P 40). WOrms without
daf-2 will lose their extra longevity if they are also missing
daf-16, a gene needed for the production of two key enzymes that
prevent cell damage - cytosolic catalase and manganese superoxide
dismutase. But how does the dof-2 pathway actually work? At the
moment it's not clear, but there are some clues. From investigations
done in Kenyon's lab and elsewhere it appears, in worms at least,
to involve neurons releasing insulin-like hormones. These trigger
the release of a second hormone that travels to cells throughout
the body. No one knows what this hormone does, but researchers
speculate that it somehow acts as a general inhibitor of the damage
limitation and repair systems.

Slowly does lt

For Kenyon, this all adds up to one thing: animals lacking
genes such as daf-2 live longer because they age more slowly.
But Hayflick and others disagree. They say there is at least one
other feasible explanation. What if longevity is being increased
because such gene mutations make individuals more resistant to
one particular cause of death - say heart disease?

To address this question, researchers are now attempting to
deftne and measure ageing in worms at the cellular level, so they
can see if the process is actually slower in long-lived mutants.
In one recent set of experiments, Delia Garigan, working with
Kenyon, identified several age-related changes in worm cells.
These included a gradual blurring of the boundary ofthe cell nucleus
and a change in the texture of cytoplasm from smooth to curdled.
Garigan also noted a correlation between these changes and the
loss of mobility that also strikes aged worms. Next, Garigan looked
at cells from daf-2 mutant worms and saw a delay in the signs
of ageing. Nuclear boundaries for instance, remained visible for
approximately 2o days, whereas in normal worms they disappeared
after only five days.

The researchers who accept that a single genetic pathway can
affect ageing, are now arguing over whether such a process evolved
specifically to cause ageing. Those who think it did not argue
that the ageing pathway is compatible with existing evolutionary
theories that see ageing as the price paid for successful reproduction.
According to this idea, animals faced with food shortages undergo
changes that include storing more fat, delayed reproduction and
a ramping up of the mechanisms that maintain, repair and protect
cells from molecular damage. Proponents of this view see delayed
reproduction as the primary effect of the survival mechanism,
and added longevity as a secondary effect. Evidence for this view
comes from experiments showing that when large numbers of flies
are selectively bred to lay eggs when young, their lifespans shorten
over the generations, while those bred to lay eggs when they are
older live longer. What's more, the price of the trade-off is
evident in the extreme side-effects experienced by most long-lived
mutant organisms. These range from complete or partial disruption
in fertility, to dwarfism. "I really don't believe there
is a set of genes that are designed to make you age," says
Monica Driscoll, a geneticist at Rutgers University in Piscataway,
New jersey. "There are certain genes that contribute to how
you age. But the idea of a program analogous to what you have
for development is probably not right.' But another recent set
of experiments from Kenyon's lab seems to support the idea that
this genetic pathway evolved, at least partly, to promote ageing.
Andrew Dillin turned down daf-2 activity in normal worms until
they reached young adulthood, when he returned it to normal.

"I'm startingto like the idea that it s ops animals from
competing with their young'

He discovered that these animals experienced the same reduced
fertility as in daf-2 mutants, but failed to live longer. But
when he disrupted dof-2 after the normal worms reached adulthood,
the animals lived as long as daf-2 mutants but without the accompanying
reduction in fertility. This suggests that the daf-2 signalling
pathway's control over longevity is separate from its effect on
reproduction. Kenyon thinks this points to a separate genetically
determined ageing program. Perhaps Wallace was right after all.
"Why does daf-2 remain active during adulthood, if the only
apparent effect of its action is to speed up ageing?" says
Kenyon. "I'm starting to like the idea that it prevents animals
from competing with their young.' There is also growing doubt
over whether a trade-off is always a necessary condition of added
longevity. The long-lived IGF-I n-dce seemed normal in almost
every way: normal body temperature, normal circadian rhythms,
normal metabolism, normal litter sizes, normal number of pregnancies,
normal onset of infertility. The only difference was a slight
reduction in size. In females, this size reduction was eight per
cent, not a bad swap for a lifespan extended by a third.

While this debate remains up in the air, there are researchers
from both sides who are now prepared to say it's wrong to view
ageing as a process that can't be altered. The powerful effects
that genes appear to have on the body's ability to withstand the
ravages of time, whether or not they actually evolved for that
purpose, suggest that a fountain of youth may be out there after
all. The trick is to find it.

Garry Hamifton is a freelance science writer living in Seattle,
Washington

Asteroids - are we doing Enough?

We are monitoring the skies for asteroids on a collision course
with Earth,and the public isbeginning to realise the devastation
an impacy could cause. But is this enough?In thefollowing pages
we look at the latest predictions of what mighthappen if disaster
strucl(, and what could be done to avert an impact if we saw it
coming. Butfirst,ErikAsphaug, an expertin modellingplanetary collisions,tal(esa
critical look at theprecautionsalready in place, andconcludes
that it'stime to stop playing around.

SOMETIME in the next lo,ooo years an enormous rock will crash
into an ocean, and loo-metre waves will radiate out to flood coastal
cities and distant lowlands. The human toll could be tens of millions
of lives, and the economic loss could be measured in trillions
of dollars. I am talking about the impending collapse of Cumbre
Vieja, the unstable southem flank of the island of La Palma, part
of the Canaries in the western Atlantic. The geological record
shows that collapses of this magnitude occur about every 2o,ooo
years, whereas asteroids or comets large enough to produce comparable
waves strike Earth only a fifth as often. Indeed, the impact of
a near-Earth object, or NEO - an asteroid or comet whose orbit
comes close to Earth - represents just one of several low-probability,
high-consequence calamities that can befall humankind. Topping
the list may be warfare, plague and ecological collapse triggered
by human disregard. So why, if these other threats are greater,
should we care about hazardous NEOS? Beyond their broad and novel
appeal to space buffs and doomsayers alike, there are rational
motives for designing strategies to deal with hazardous comets
and asteroids. Quite unlike any other natural disaster, the NEO
risk can be reduced almost to zero through achievable, feasible
means. Indeed, the most dangerous NEOs could even benefit mankind.
If we could move them to safe nearby orbits, they would be readily
accessible outposts for human exploration and exploitation, science
fiction made real. We cannot do much about volcanoes or earthquakes
other than identify active regions and tell people not to build
there. But cataclysmic asteroids are predictable: given sufficient
lead time and a precisely determined trajectory, a tiny diversion
applied decades in advance can change the future. Isaac Newton,
inventor of the clockwork heavens, knew of gravitational perturbation,
and argued that God had to occasionally nudge the orbits of comets
to prevent them from eventually colliding with Earth. Perhaps
it is our role to keep the wayward comets and asteroids on track.
Today, of the $4 million spent annually on investigating NEOS,
almost all goes towards detection and orbit prediction. The process
of asteroid detection has far outpaced the scientific understanding
of what asteroids are, and what we can do about them. This is
partly because no govemment agency deals with hazardous NEOs in
any direct way, other than counting them and cataloguing their
orbits. It is easy to list the national and worldwide agencies
that deal with volcanic eruptions, earthquakes, tsunamis, disease,
famine and warfare. Indeed, many agencies exist solely to deal
with a particular hazard. But while many (including Hollywood)
assume that NASA is in charge of NEO defence, NASA has no such
mandate. Neither does the US Air Force or any other agency. NEOs
fall into the cracks: they are a hazard without a home. NASA and
space agencies in Europe and japan do, however, play a leading
role in ftindamental exploration of asteroids and comets. We now
know that they are surprisingly complex entities. Indeed, we have
figured out that we wouldn't know how to divert one even if some
agency were in cha@ge. Until recently, the favoured NEO diversion
scenario was a blast from a nuclear explosion (see page 38). But
new data have shown that many asteroids are not solid rocks but
loosely connected multi-component objects - rubble piles, in fact.
This makes them very hard to disrupt or move predictably by impulsive
force. By doing no more than detecting asteroids, or treating
them as geophysical curiosities, we are generating increasing
concem without following through with a plan. Because of uncertainties
in measuring their orbits, asteroids that have a finite initial
chance of hitting Earth sometime down the road are frequently
discovered. Collision is almost always ruled out by follow-up
observations, but not before we read in the moming paper that
we all are doomed. The painful irony is that these detection programmes
should be making the public feel tangibly safer. Thanks to ceaseless
efforts at a handful of small observatories, half of the kilometre-sized
NEOs have been logged, and none is on a collision course with
Earth: we can feel twice as safe as we did. With sufficient effort
in the form of larger telescopes, and significant funds for observations
and follow-up research, we could soon have nearly all the hazardous
rocks in the heavens tracked in a celestial version of air traffic
control. Most likely (a thousand to one) this survey, when completed,
would signal the all-clear for any object larger than 300 metres
across headed for a collision within a century. But if we are
gravely unlucky and we find something large is headed our way,
we would want to do better than finding the biggest rocket available
and strapping on the biggest nuclear warhead it could carry. This
may not work, and it's a scenario appropriate only to an unprepared
civilisation scrambling for a last- minute solution. The purpose
of a detection effort is hopefully to signal the all-clear, and
failing that, to buy us the long lead time required to engineer
a reliable and cost-effective deflection strategy. It must be
accompanied by a growing understanding of how to apply a small
diversion to an asteroid. It is not going to be easy, unless you
compare it with other space-related endeavours such as visiting
the Moon. The basic research requires ambitious spacecraft missions
to determine detailed geological characteristics for a wide range
of comets and asteroids. This will not come cheap, unless you
measure it in military metrics. For the cost of a single B2 bomber,
we could launch a major NEO geophysical reconnaissance mission
(at about $300 minion per mission) every five years for the next
30 years. This would take us from this place of ignorance to one
where clear decisions can be made - and where a future human presence
in near-Earth space is all but certain. We cannot afford spacecraft
exploration ff it means diminished asteroid surveillance. But
we are clearly at the stage where surveillance alone will not
do. With surveillance comes the public expectation that we have
a plan for Teaming more about hazardous NEOS, including how to
divert one. But we are scrambling for a plan, for funding, and
for an agency to take on this difficult charge.

Erik Asphaug is associate professor of earth silences at the
University of Califbmia, Santa Cruz

THANKS to Hollywood, we already know what to do if an asteroid
big enough to wipe out life on Earth is spotted coming our way.
Haul out our surplus nuclear weapons and get Bruce Winis on the
phone.

But there's a catch. In the past year, asteroid researchers
have been warning that it would be a big mistake to rely on nuclear
bombs to save the planet. Nuking a killer asteroid as it approaches
could be the worst thing our superhero could do, even compared
with doing nothing. In February, asteroid researchers submitted
a report to NASA headquarters in Washington DC calling for more
research into deflection technologies that are a far cry from
the "all guns blazing" approach. If they have their
way, our toolbox for saving the planet will include ways of gently
coaxing the killer into a safe orbit, either by slowing its irregular
spin, by giving it a whitewash or even by parcelling it up in
wrapping paper. At first glance, blowing a killer asteroid to
smithereens seems like a good idea. Asteroids a kilometre across
- the size that threaten the future of our civilisation - should
be no match for a io-megaton nuclear bomb, among the largest in
current arsenals. Push the red button with several months to spare
and the debris should disperse in time. "You get one hell
of a meteor display on the night that was previously going to
be Armageddon," says Alan Harris, an asteroid researcher
who retired last year from NASA's Jet Propulsion Laboratory in
Pasadena, California. But as fans of the movie Armageddon know,
simply firing a warhead at the asteroid and exploding it on the
surface won't destroy it. Our heroes will need to land on the
rock and bury the bomb at least ioo metres deep. This is bound
to be a high-risk strategy, however, because getting the depth
and digging technique right for an unknown material will be fraught
with difficulty. Get it wrong and you risk creating a blast of
chunky shrapnel that wfll spread more devastation across the planet
than a localised collision. These concems have led researchers
to consider using a nuke to deflect rather than destroy an asteroid.
Deflection depends on transferring lots of sideways momentum,
rather than explosive energy, to the asteroid. Detonating a bomb
on the surface will only vaporise a small portion of the asteroid,
but detonating a nuclear bomb well above the surface - about 200
metres for a i-kilometre asteroid - will vaporise a greater mass.
As the mass is blown off the surface, the rest of the asteroid
will gain an equal amount of momentum in the opposite direction.
A bomb with a kick ofbetween loo kilotons and i megaton, detonated
200 metres above the surface of a solid asteroid a kilometre across,
should vaporise the top 20 centimetres- This would be enough to
give it a sideways shove that would change its velocity in this
direction by about io centimetres per second. That would ensure
a miss, given seven years'notice.

Unfortunately, this now also looks tricky. In 2002, a series
of optical and radar images taken from Earth and from probes overthrew
a key assumption underpinning these calculations. Instead of being
solid rocks, most asteroids are porous piles of rubble barely
hanging together in space. As many as one in six known asteroids
is not even doing that. They are binaries - two rubble piles orbiting
each other.

This disturbing discovery led Keith Holsapple of the University
of Washington in Seattle to study the effect of nuclear nudges
on porous rubble piles. "A very porous material is very effective
at absorbing energy," Holsapple says. Push hard on a rock
and it moves; push hard on a porous material and it crushes like
polystyrene packing material. Holsapple cakulates that a megaton
nuclear blast 200 metres away would push a 1-kilometre rubble-
pile asteroid only a thousandth as effectively as it would a solid
body. So to deflect a i-kilometre asteroid you'd need a 1-megaton
blast up close, says Holsapple. To deflect a lo-kilometre asteroid
like the one that saw off the dinosaurs, you'd need a 1-gigaton
bomb - a hundred times more powerful than any ever tested. Holsapple's
work has prompted a change in tactics. At NASA's Workshop on Asteroid
Mitigation last September, no one was talking about nukes. Instead,
the motto behind many of the ideas was "softly- softly".
Several researchers proposed using engines that would thrust gently
for a long time, rather than explosively. Former astronaut Rusty
Schweickert talked about landing an ion rocket engine on the asteroid
and using it to shunt the asteroid gradually to the side. Such
engines use solar energy or a small nuclear reactor to heat propellant
slowly and eject it continuously, producing a thrust so gentle
that the object's delicate structure should not matter. Schweickert
is chairman of the B612 Foundation (named after the home planet
of the Little Prince in Antoine de Saint-Exup6ry's book of the
same name). The private group, based in Houston, hopes to persuade
a consortium of NASA and private funders to let them try changing
the orbit of a loo-metre rubbly asteroid by 2015. As well as designing
the propulsion system, the group is planning the delicate space
operations needed to pick a landing site, dock there and begin
to push the asteroid. "You don't have to use a lot of fuel,
but you have to use a lot of brains," says Schweickert. Asteroids
typically spin on their axis as well as orbiting the Sun. So to
push an asteroid in one direction rather than simply increasing
or decreasing its spin, an engine on the surface could fire only
once per rotation. Instead Schweickert says the engine will land
on the equator, line up with the asteroid's spin, then fire in
the opposite direction. With an asteroid completing one rotation
in a few hours, an ion engine should take several months to a
year to stop it spinning. The engine can then swivel through go'
and push the asteroid continuously in one particular direction.
But the asteroid's rotation may not be known precisely, so researcher
lay Melosh of the University of Arizona favours an altemative
approach. He suggests using a "solar concentrator" -
a giant parabolic mirror - to focus sunlight onto the asteroid's
surface. As the asteroid spins, the light and heat should evaporate
material from whatever part of the surface happens to fall in
the focal spot. As long as the light is shone at a constant angle
to the surface, the gradual momentum gain by evaporating material
will move the asteroid gently in the opposite direction. To steady
the mirror's position against the force of the solar wind, which
would be significant on a large mirror, a low-thrust rocket engine
- similar to those being developed by the B612 Foundation - would
be needed. Jim Pawlowski, a specialist in asteroids and orbital
debris who has just retired from NASA's Johnson Space Center in
Houston, estimates that a 32-metre mirror would take lo years
to deflect a typical i-kilometre near-Earth asteroid from its
destructive course.

Ideally, researchers would prefer a scheme that, like a nuclear
explosion, only required a one-off intervention, but that moved
the asteroid very gently over a long time. One idea is to change
how much light the asteroid reflects in order to change its orbit.

The orbits of asteroids aren't just determined by the gravitational
forces in the Solar System; other effects also play a part. The
@unlit side of a dark asteroid continuously absorbs light energy
from the Sun. The momentum ofthe solar photons is transferred
to the asteroid, altering its orbit continuously by an amount
that

depends on how well it absorbs the light. There is also a second,
less obvious phenomenon. As the asteroid rotates, the "Yarkovsky
effect" comes into play. Several hours after having the Sun
directly overhead, the surface re-emits absorbed energy in the
infrared. The asteroid effectively donates some momentum to the
infrared photons, and recoils, altering its orbit. This sets the
stage for a big idea. Most asteroids are so dark they absorb all
but a few per cent of the incident light, but if they were coated
with something shiny or white, the light would bounce off instead.
If the energy is not absorbed, it cannot be emitted later. So
a whitewash would all but remove the Yarkovsky effect on the asteroid's
orbit. In the absence of the effect, a typical killer near-Earth
asteroid will be deflected by a few millimetres per second from
the path it would have taken. Over a couple of centuries, that
would be enough for it to miss the Earth. But how could we possibly
hope to change an asteroid's surface properties? Compared to timing
a nuke or training a solar concentrator, it is relatively easy,
says Jon Giorgini of the jet Propulsion Laboratory. Splatting
the surface with white paint could do it, but the quantity needed
would be heavy and expensive to transport to the asteroid's orbit.
More likely, reflective glass beads or a white powder, such as
chalk dust, would be fired into the asteroid's gravitational field.
Because the field is so irregular, the particles would bounce
to ground over a variety of different trajectories, eventually
covering the entire surface. But to make the covering really even,
Giorgini favours a solar sail. If a giant piece of reflective
material were unfolded in the path of the asteroid, it could be
made to envelop it, covering the whole thing like a giant birthday
present. "It's technology we could do now," says Giorgini,
although it will take centuries to work. Not everyone is convinced
by the potential for the Yarkovsky effect to save the planet.
"Exactly how efficient it is remains to be learned,"
says Mike Belton, co-organiser of the NASA workshop and head of
Belton Space Exploration Initiatives in Tucson, Arizona. Part
of the problem is that the Yarkovsky effect is smaller than the
uncertainties in many asteroid's orbits. This means that even
if researchers think a rock is on course for us, they may not
know whether changing the Yarkovsky effect on it would be enough.
Even proponents of prospective schemes agree that developing them
into a real toolbox of alternatives could take decades. And there's
no time to lose. Although none of the currently known 48o or so
near-Earth asteroids over 1 kilometre in size is classed as hazardous,
imprecision in measuring their orbits makes it impossible to predict
this more than a century into the future. One exception is asteroid
195oDA, which orbits unusually far from other perturbing objects
and in such a way that the gravitational effect of the Earth on
it varies in a simple, regular way, a phenomenon known as a resonance.
If 195oDA is spinning in one particular direction - and we don't
actually know how it is spinning - there is a i in 300 chance
it will hit the Earth on 16 March 288o. If it spins the other
way, the Yarkovsky effect on it will be different and it is sure
to miss. As surveys continue, they are likely to tum up other
relatively high-risk candidates for astronomers to keep an eye
on. But if all goes according to plan, by the time we find our
first killer asteroid we will be ready with a shiny coat to send
it on its way. Saving humanity with baking foil may not seem as
daring as blasting the asteroid to kingdom come, but if it works,
not even Hollywood will complain.